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Eye movements lecture
A/P Uma's lecture. For slides go to:Public Folder, http://public.me.com/umapathi password: ONE-learn Failure of abduction of one eye - Muscle *Paralysis of lateral rectus *Restriction of medial rectus - Neuromuscular junction: Myasthenia gravis - Peripheral nerve Prof Loong's original rules of cranial neuropathy 1. All come from the brainstem except for CN 1 and 2. *midbrain: CN 3 & 4 *pons: CN 5, 6 & 7 *ponto-medullary junction: CN 8 *medulla: CN 9, 10, 11 & 12 2. All must pass through the meninges/base of the skull as they exit the brainstem. *Can be affected in meningitis or meningeal metastases. *For CN 6, it is usually one of the first nerves to be affected in nasopharyngeal carcinoma. NPC can present with lateral rectus palsy due to local infiltration along the base of the skull. 3. Remember the cranial nerve clubs: *CN 3, 4, 5 & 6: cavernous sinus (can be solely CN 6 as it is usually the first one affected), superior orbital fissure *CN 2, 3, 4 & 6: orbital apex *CN 5, 6, 7, 8 and cerebellum: cerebellopontine angle *CN 9, 10 & 11: jugular foramen *CN 9, 10 & 12: bulbar palsy 4. Remember Guillain Barre syndrome (and its variant Miller Fisher Syndrome), the most important polyneuropathy that simultaneously affects cranial nerves. Thyroid eye disease: *Sympathetic signs: lid lag, lid retraction *Infiltrative signs: extraocular muscle movement restriction, exopthalmos Internuclear ophthalmoplegia: Lesion disrupts the medial longitudinal fasciculus (MLF) in the midbrain, causing weakness in adduction of ipsilateral eye with nystagmus of contralateral eye only when it is abducting. Why nystagmus? Think of it as over-stimulation of normal eye when brain is trying to get the abnormal eye to adduct in horizontal gaze, causing 'over-shooting' of normal eye= 'ataxic nystagmus'. Where is the lesion? If convergence is preserved, more likely pontine than midbrain (convergence center is in midbrain). Bilateral internuclear ophthalmoplegia: likely in midline of brainstem, usually midline pontine. Causes: basilar artery disease, germ cell tumor (common in children). Left gaze palsy (inability to look to the left): Causes: *Lesion at left 6th nucleus: (lateral gaze center: contains cell bodies for left 6th nerve and interneurons for MLF of right eye). Patient looks toward his hemiplegia. *Lesion at right frontal eye field (loss of supranuclear control of gaze to contralateral side). Patient looks away from his hemiplegia. To differentiate: Doll's manoeuvre. If impaired (aka loss of VOR), likely to be pontine. Also look for signs of right frontal lobe and left pons. Vestibulo-ocular reflex From ear (to vestibular nucleus) to contralateral 6th nucleus. If impaired, causes peripheral nystagmus. Fast component is the correction back to central gaze. Eg. If lesion is on left: there is decreased signals from left ear. Brain interprets this imbalance as increased signals from right ear, i.e as if head is turning to right, so eyes will drift towards the abnormal ear (slow phase nystagmus). Corrective saccades back to central gaze, ie fast phase away from lesion. Peripheral nystagmus is due to vest imbalance and hence does not change direction, and can occur in primary gaze. Peripheral nystagmus can be worse on eye closure due to loss of visual input to compensate for imbalance of vestibular signals. One and a half syndrome (Bilateral INO with failure of abduction of one eye) Scenario: Patient has right gaze palsy and only left eye can abduct. = Lesion of 'ipsilateral MLF and right 6th nucleus OR ipsilateral MLF and right '''PPRF' '('''Paramedian pontine reticular formation) '''PPRF': Paramedian pontine reticular formation = Connects frontal eye field to contralateral 6th nucleus for generation of HORIZONTAL saccades. Located anterior and lateral to MLF. Analogy for different kinds of complex eye movements: Hunter in forest, looks ahead but needs to be aware of surroundings: Peripheral vision (only aware of movements but not details of objects in periphery) Notices something moving in periphery, looks to locate object quickly: Saccades (quick movement of eye from one spot to another, without noticing details of the interim) Spots an antelope, tracks its movements to try to hunt it down: Pursuits (smooth movement of the eye as it tracks a moving object) Runs after antelope, VOR (vestibular ocular reflex) allows hunter to "foveate" on the target reflexly; also looks at surrounding changing landscape while running: Optokinetic movements (movements of eye as it follows for eg, moving numbers on a measuring tape as it is pulled) Finally catches up with the antelope, aiming for the kill by trying to locate the jugular vein: Convergence (eyes trying to focus on a near object) Burst neurons ''(go-there neurons)'' are needed to generate the saccades. Therefore, with a "go-there" problem, there are saccadic intrusions. But to maintain the gaze, stay-there neurons (neural integrators-''' located in brainstem/ cerebellum) are needed. Therefore, with a "stay-there" problem, there is nystagmus. '''Central nystagmus= gaze-evoked, multidirectional nystagmus. It is nystagmus seen in both eyes in all directions of gaze, when looking to the right, left, upward and downward. It is typically due to impaired neural integrators. Cerebellar eye signs (covered in Grand Ward Round 8th April 2010) *Gaze-evoked multidirectional nystagmus *Loss of smooth pursuit **ask patient to follow pen tip as you move it slowly from left to right **jerky eye movements is analogous to intention tremor when doing finger-nose test *Saccadic dysmetria **ask patient to quickly switch gaze from left object to right object and back again **Patient tends to initially focus either to the left or the right of the object (over-shoot, under-shoot) before consciously shifting the gaze to the object finally **analogous to past-pointing when doing finger-nose test NB: Slow saccades (i.e inability to quickly switch gaze from 1 object to another) is not a cerebellar sign per se but an indication of pathology in the saccade generator eg the PPRF. This is seen in spinocerebellar ataxia Type 2